Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects.

Elshout, F. J. van den; Herwaarden, C L van; Folgering, H.T.M.

doi:10.1136/thx.46.1.28

Cited by 114 publications

(56 citation statements)

References 24 publications

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“…When NEWHOUSE et al [123], for example, raised the minute ventilation in five normal males to 30 L?min -1 and dropped the PA,CO 2 to 2.7-3.3 kPa (20-25 mmHg), mean inspiratory flow resistance increased by 133% and mean respiratory work increased by 68% when compared with a minute ventilation that yielded a PA,CO 2 of 6.0-6.7 kPa (45-50 mmHg). Similarly, VAN DEN ELSHOUT et al [124] examined asthmatic patients with impulse oscillometry and found that a 1.0-kPa (7.5-mmHg) fall in the end-tidal carbon dioxide tension led to a 13.2% increase in airway resistance and a 45% fall in airway reactance.…”

Section: Hypocapniamentioning

confidence: 98%

“…This response is potentially problematic in asthmatic patients because hypocapnia has been shown to adversely affect airway resistance [123][124][125][126]. When NEWHOUSE et al [123], for example, raised the minute ventilation in five normal males to 30 L?min -1 and dropped the PA,CO 2 to 2.7-3.3 kPa (20-25 mmHg), mean inspiratory flow resistance increased by 133% and mean respiratory work increased by 68% when compared with a minute ventilation that yielded a PA,CO 2 of 6.0-6.7 kPa (45-50 mmHg).…”

Section: Hypocapniamentioning

confidence: 99%

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Travel to high altitude with pre-existing lung disease

Luks

Swenson²

2007

Eur Respir J

107

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The pathophysiology of high-altitude illnesses has been well studied in normal individuals, but little is known about the risks of high-altitude travel in patients with pre-existing lung disease. Although it would seem self-evident that any patient with lung disease might not do well at high altitude, the type and severity of disease will determine the likelihood of difficulty in a high-altitude environment. The present review examines whether these individuals are at risk of developing one of the main forms of acute or chronic high-altitude illness and whether the underlying lung disease itself will get worse at high elevations. Several groups of pulmonary disorders are considered, including obstructive, restrictive, vascular, control of ventilation, pleural and neuromuscular diseases. Attempts will be made to classify the risks faced by each of these groups at high altitude and to provide recommendations regarding evaluation prior to high-altitude travel, advice for or against taking such excursions, and effective prophylactic measures.

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Section: Hypocapniamentioning

confidence: 98%

Section: Hypocapniamentioning

confidence: 99%

Travel to high altitude with pre-existing lung disease

Luks

Swenson²

2007

Eur Respir J

107

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“…[4-81. Bronchoconstriction also occurs in animals when carbon dioxide tension is reduced acutely [9, 101. In humans, hyperventilation asthma has been recognized for at least half a century [ll] and an acute fall in end-tidal carbon dioxide (ETCO2) of 7.5 mmHg has also been shown to contribute to airway obstruction in asthmatic patients [12] and patients undergoing hyperventilation (mean PaCOz 30.4 mmHg) because of neurological injury [13]. In normal subjects, acute hypocapnia (PaCOz 20-25 mmHg) also causes a consistent increase in flow resistance during sustained voluntary hyperventilation [14].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia, Hypocapnia and Spirometry at Altitude

et al. 1997

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1. Both hypoxia and hypocapnia can cause broncho-constriction in humans, and this could have a bearing on performance at high altitude or contribute to altitude sickness. We studied the relationship between spirometry, arterial oxygen saturation and end-tidal carbon dioxide (ETCO2) concentration in a group of healthy lowland adults during a stay at high altitude, and then evaluated the response to supplementary oxygen and administration of a beta 2 agonist. 2. We collected spirometric data from 51 members of the 1994 British Mount Everest Medical Expedition at sea level (barometric pressure 101.2-101.6 kPa) and at Mount Everest Base Camp in Nepal (altitude 5300 m, barometric pressure 53-54.7 kPa) using a pocket turbine spirometer. A total of 205 spirometric measurements were made on the 51 subjects during the first 6 days after arrival at Base Camp. Further measurements were made before and after inhalation of oxygen (n = 47) or a beta 2 agonist (n = 39). ETCO2 tensions were measured on the same day as spirometric measurements in 30 of these subjects. 3. In the first 6 days after arrival at 5300 m, lower oxygen saturations were associated with lower forced expiratory volume in 1 s (FEV1; P < 0.02) and forced vital capacity (FVC; P < 0.01), but not with peak expiratory flow (PEF). Administration of supplementary oxygen for 5 min increased oxygen saturation from a mean of 81%-94%, but there was no significant change in FEV1 or FVC, whilst PEF fell by 2.3% [P < 0.001; 95% confidence intervals (CI) -4 to -0.7%]. After salbutamol administration, there was no significant change in PEF, FEV1 or FVC in 35 non-asthmatic subjects. Mean ETCO2 at Everest Base Camp was 26 mmHg, and a low ETCO2 was weakly associated with a larger drop in FVC at altitude compared with sea level (r = 0.38, P < 0.05). There was no correlation between either ETCO2 or oxygen saturation and changes in FEV1 or PEF compared with sea-level values. 4. In this study, in normal subjects who were acclimatized to hypobaric hypoxia at an altitude of 5300 m, we found no evidence of hypoxic broncho-constriction. Individuals did not have lower PEF when they were more hypoxic, and neither PEF nor FEV1 were increased by either supplementary oxygen or salbutamol. FVC fell at altitude, and there was a greater fall in FVC for subjects with lower oxygen saturations and probably lower ETCO2.

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“…Changes in blood gas tension can be another sources of influence on the airways. The fall in PCO 2 related to hypocapnia has bronchoconstrictive effects, but there is conflicting evidence on effects of hypercapnia and hypoxia~Si-mon, Zanaboni, & Nyhan, 1997;van den Elshout, van Herwaarden, & Folgering, 1991!. Recommendation. Continuous measurements of ventilation should be included in psychophysiological studies of mechanical lung function.…”

Section: Ventilationmentioning

confidence: 99%

Guidelines for mechanical lung function measurements in psychophysiology

Ritz¹,

Dahme²,

DuBois³

et al. 2002

Psychophysiol.

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Studies in psychophysiology and behavioral medicine have uncovered associations among psychological processes, behavior, and lung function. However, methodological issues specific to the measurement of mechanical lung function have rarely been discussed. This report presents an overview of the physiology, techniques, and experimental methods of mechanical lung function measurements relevant to this research context. Techniques to measure lung volumes, airflow, airway resistance, respiratory resistance, and airflow perception are introduced and discussed. Confounding factors such as ventilation, medication, environmental factors, physical activity, and instructional and experimenter effects are outlined, and issues specific to children and clinical groups are discussed. Recommendations are presented to increase the degree of standardization in the research application and publication of mechanical lung function measurements in psychophysiology.Descriptors: Mechanical lung function, Airway resistance, Respiratory resistance, Spirometry, Pneumotachography, Body plethysmography, Forced oscillation technique, Interrupter technique, Respiratory perception Despite long-standing interest in respiration by psychophysiologists, it is surprising that little attention has been directed to methodological issues of specific measurement techniques in this area. Although occasional textbook chapters have been devoted to respiration measurements, a more in-depth discussion of techniques dealing with the assessment of mechanical lung function is still missing. Mechanical lung function relates to lung volumes and airflow through the respiratory system as well as the pressurevolume and pressure-flow characteristics as indicators of elastic and resistive properties of the airways, lungs, and chest wall. In clinical practice, mechanical lung function measures are widely used for the diagnosis and management of various pulmonary diseases, most importantly bronchial asthma and chronic obstructive pulmonary disease~COPD!. In psychophysiology and behavioral medicine, potential associations between psychological or behavioral processes and mechanical lung function offer an exciting perspective both for basic research and clinical application. Due to the particular importance of the vagal system in governing airway function, the airways offer a unique window into the autonomic nervous system regulation of behavior, emotion, and cogThomas Ritz acted as coordinator and contributor to this report. The authorship of the other contributors was determined by alphabetical order. Different sections were drafted by individual contributors, submitted to internal peer review, and revised until consensus was achieved. We are indebted to

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Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects.

Cited by 114 publications

References 24 publications

Travel to high altitude with pre-existing lung disease

Travel to high altitude with pre-existing lung disease

Hypoxia, Hypocapnia and Spirometry at Altitude

Guidelines for mechanical lung function measurements in psychophysiology

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